Transformation of mammalian cells is a useful model system for viral oncogenesis. Little is known about what factors govern the difference in response of different cell (species) types to viruses--whether the cell will be killed or transformed, whether virus will replicate its DNA, be transcribed, have viral DNA integrated into cell DNA or completely degraded. Various serotypes of human adenoviruses differ in their interactions with given cell types at the level of DNA replication, and specifically with the amount of defective genomes which are generated. I am studying the synthesis of viral DNA, complete and defective, in a variety of combinations of cell types and virus serotypes and the eventual transformation of some cells by virus. The goals of this research are to understand the nature of the primary events which determine whether or not a cell will be transformed, and to test the hypothesis that defective genomes play a specific role in transformation. I am emphasizing a systematic study of virus-cell interactions which have been studied haphazardly, heretofore, by different researchers by techniques different enough to make comparison difficult.